Serotonin and cAMP induce excitatory modulation of a serotonergic neuron.

Serotonin (5-HT) is an excitatory neurotransmitter and neuromodulator. In the Aplysia nervous system it increases excitability and induces spike broadening in sensory neurons. It is released at the synaptic terminals of the metacerebral cells (MCCs) and modulates the feeding neural circuit and buccal muscles during the aroused feeding state.

Serotonin, nitric oxide and histamine enhance the excitability of neuron MCC by diverse mechanisms.

Serotonin, nitric oxide (NO) and histamine are neuromodulators used in molluscan nervous systems. We have found that each of them depolarizes and increases the excitability of the serotonergic feeding neural circuit modulator neuron, MCC, of Aplysia, but each induces different changes in background ionic currents and uses a different second messenger. Stimulation of neuron C2 in the cerebral ganglion induces a vsEPSP in MCC using NO and histamine.

Nitric oxide and histamine induce neuronal excitability by blocking background currents in neuron MCC of Aplysia.

Nitric oxide (NO) and histamine are important neurotransmitters and neuromodulators. We investigated their ability to modulate the membrane ionic currents and excitability of the metacerebral cell (MCC) of Aplysia using voltage clamp techniques. MCC is a serotonergic modulator of the feeding neural circuit.

Nitric oxide induces cGMP immunoreactivity and modulates membrane conductance in identified central neurons of Aplysia.

Nitric oxide (NO) acts as an orthograde neurotransmitter in the central nervous system by stimulating guanylyl cyclase and increasing cGMP. We previously demonstrated this pathway for an identified synaptic follower neuron in the cerebral ganglion of the mollusc Aplysia californica. Here, we investigated the NO--cGMP pathway in other Aplysia central neurons using cGMP immunocytochemistry and intracellular recordings.

Nitric oxide stimulates cGMP production and mimics synaptic responses in metacerebral neurons of Aplysia.

Nitric oxide (NO) acts as a neurotransmitter and neuromodulator in the nervous systems of many vertebrates and invertebrates. We investigated the mechanism of NO action at an identified synapse between a mechanoafferent neuron, C2, and the serotonergic metacerebral cell (MCC) in the cerebral ganglion of the mollusc Aplysia californica. Stimulation of C2 produces a decreasing conductance, very slow EPSP in the MCC.